Abstract
Telomeres, the short repeated sequences at the ends of chromosomes, are maintained by the telomerase DNA replication complex. In telomerase-deficient cells, telomere shortening occurs until cell proliferation halts, a process called senescence. The precise cause of senescence is unknown, but several models have been proposed. For example, cells may form lethal chromosome rearrangements, the shortened chromosomes may lose essential genes from the ends, or programmed cell death (apoptosis) may be initiated. Alternatively, cells may simply arrest growth in the cell cycle, but remain viable for an extended period of time. Telomerase-deficient cells of the model eukaryote Saccharomyces cerevisiae undergo telomere shortening and senescence in culture. This study has used the advanced molecular genetics available in this organism to investigate the mechanism by which senescing cells halt division. Unique strains of S. cerevisiae have been developed in the lab that allows precise regulation of expression of the polymerase subunit of telomerase Est2. With these strains it is possible to reactivate telomerase expression at any stage of the senescence process, potentially enabling dying cells to lengthen their telomeres and resume growth. Recent experiments suggest that in vitro cell aging is reversible in most cells, even in late senescence. These results and their implications for previously suggested models will be discussed.
Published Version
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